| First Author | Ding LC | Year | 2017 |
| Journal | Oncotarget | Volume | 8 |
| Issue | 29 | Pages | 48098-48109 |
| PubMed ID | 28624805 | Mgi Jnum | J:259652 |
| Mgi Id | MGI:6148139 | Doi | 10.18632/oncotarget.18259 |
| Citation | Ding LC, et al. (2017) Rcan2 and estradiol independently regulate body weight in female mice. Oncotarget 8(29):48098-48109 |
| abstractText | Rcan2 increases food intake and plays an important role in the development of age- and diet- induced obesity in male mice. However, in females, wild-type mice grow almost at a similar rate as Rcan2-/- mice on normal chow diet from 6 weeks of age. Here we showed that the ability of Rcan2 to promote weight gain was attenuated by energy expenditure mediated by 17beta-estradiol in female mice. Using ovariectomy-operated models, we found that 17beta-estradiol deprivation did not alter food intake, but induced more weight gain in wild-type mice than Rcan2-/- mice. If wild-type mice ingested equally as Rcan2-/- mice, in the same ovarian state they exhibited similar weight changes, but the mice in ovariectomized groups were significantly heavier than the ovarian-intact mice, suggesting that body weight is not only regulated by Rcan2, but also by 17beta-estradiol. Furthermore, we demonstrated that Rcan2 and 17beta-estradiol independently regulated body weight even on high-fat diets. Therefore, our findings indicate that Rcan2 and 17beta-estradiol regulate body weight through different mechanisms. Rcan2 increases food intake, whereas 17beta-estradiol promotes energy expenditure. These findings provide novel insights into the sexual dimorphism of body weight regulation. |
